Molecular Mimicry in HLA-B27-Related Arthritis

  1. David T.Y. Yu, MD;
  2. S. Yoon Choo, MD; and
  3. Terry Schaack, MD
    • Current Author Addresses: Drs. Yu and Schaack: Department of Medicine, Division of Rheumatology, UCLA School of Medicine, Los Angeles, CA 90024.

      Dr. Choo: Fred Hutchinson Cancer Research Center, 1124 Columbia Street, Seattle, Washington 98104.

    Abstract

    A unique feature of patients with ankylosing spondylitis and reactive arthritis is that almost all share the HLA type B27. The primary structures of the HLA-B27 antigens have been determined. At least six variants exist. However, disease predisposition does not appear to be restricted to a particular variant. One hypothesis about the pathogenesis of arthritis is that the bacteria that cause the arthritis carry components that are cross-reactive with HLA-B27 antigens. Several reactive bacterial components have indeed been identified using monoclonal anti-HLA-B27 antibodies. Even more striking is the identification, through a computerized search, of a Klebsiella protein. This protein carries a stretch of six amino acids identical to residues 72 to 77 of two of the HLA-B27 variants. A synthetic peptide carrying these six amino acids of HLA-B27 protein is reactive with serum antibodies in some patients with arthritis. With this knowledge, investigators will be able to formulate new approaches for examining the pathogenesis of HLA-B27-associated arthritis.

    Article and Author Information

    • An edited summary of an Interdepartmental Conference arranged by the Department of Medicine of the UCLA School of Medicine, Los Angeles, California. William M. Pardridge, MD, Professor of Medicine, is Director of Conferences.

    • Authors who wish to cite a section of the conference and specifically indicate its author can use this example as the form of the reference:

      Choo SY. The HLA-B27 antigen family and disease susceptibility, pp 582-584. In: Yu DTY, moderator. Molecular mimicry in HLA-B27-related arthritis. Ann Intern Med. 1989;111:581-591.

    • Grant Support: Supported in part by the Nora Eccles Treadwell Foundation and U.S. Public Health Service grant AR 36834.

    • Requests for Reprints: David T. Y. Yu, MD, Department of Medicine, Division of Rheumatology, UCLA School of Medicine, 35-40 Rehabilitation Center, Los Angeles, CA 90024.

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